UMLS:C0034065 - FACTA Search

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Query: UMLS:C0034065 (pulmonary embolism)
14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical equipoise exists regarding whether relatives of individuals with venous thromboembolism (VTE) and thrombophilia should be screened for thrombophilia. There have been no systematic attempts to summarize studies that have assessed the incidence of VTE in relatives. The purpose of this review was to systematically identify and review observational studies with thrombophilic relatives and to summarize their findings with respect to their risk of VTE. We conducted a systematic literature review and included nine observational studies meeting a priori inclusion criteria. Potentially eligible studies evaluated VTE incidence in relatives of index patients (probands) with symptomatic thrombophilia. In the four prospective studies, the incidence of VTE for asymptomatic family members with factor V Leiden ranged from 0.58-0.67% per year, 1.0-2.5% for protein C deficiency, 0.7-2.2% for protein S deficiency, and 4% for antithrombin deficiency. About half of all VTEs occurred during well-known risk periods but incidence rates were decreased by use of prophylaxis. No deaths from pulmonary embolism or fatal hemorrhages from anticoagulants were reported. The incidence of VTE was generally lower in the retrospective studies. The pooled relative risk from four retrospective studies for factor V Leiden carriers was 3.69 (CI 2.27, 6.00) and from two studies the pooled relative risk for deficiencies of protein C, protein S, and antithrombin was 10.58 (CI 5.38, 20.81). In conclusion, the risk of VTE events in asymptomatic relatives is low, but this may be an underestimate. Anticoagulant prophylaxis during risk periods appears to be of benefit but further research in this area is required.
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PMID:Risk of venous thromboembolism in relatives of symptomatic probands with thrombophilia: a systematic review. 1287 21

We assessed the clinical status after anticoagulant therapy in acute deep vein thrombosis (DVT) involving the lower limbs. Between 1994 and 2001, 139 patients suffering from acute DVT were treated with heparin therapy followed by oral anticoagulant therapy. The coagulation factor assay was done prior to any anticoagulation therapy. The duplex scan was checked serially. The mean follow-up periods was 32 +/- 19 months. There were 32 (23.0%)cases of protein C deficiency, 12 (8.6%) cases of protein S deficiency, 13 (9.4%) cases of AT-III deficiency and 11 (7.9%) cases of abnormal plasminogen level. Fourteen cases had coagulation factor abnormalities within the family. The initial lung scan showed 29 (20.9%) cases with high, 13 (9.4%) cases with intermediate and 70 (50.4%) cases with a low probability of pulmonary embolism (PE) developing. During the follow-up periods, there were 3 cases of non-fatal PE documented with chest CT scan. The patients were divided according to the extent of the thrombus; Group I (38 cases) was limited to the infrainguinal deep vein, Group II (70 cases) extended to the iliac vein and Group III (9 cases) extended to the vena cava. Partial lysis occurred in 20/35/3 (52.6/50.0/33.3%) cases and no change in 10/24/6 (26.3/ 34.3/ 66.7%) cases in Groups I/ II/ III, respectively. Deep vein valvular reflux occurred in 15/25/5 (39.5/35.7/55.6%) cases in Groups I/ II/ III, respectively. With anticoagulation therapy, most of the thrombi remained in unresolved states and there was a high rate of deep vein valvular reflux. However, there was no serious complications which affected the patients' quality of life.
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PMID:Clinical and functional assessment after anticoagulant therapy of acute deep vein thrombosis involving the lower limb. 1295 Jan 26

Venous thromboembolism (VTE) occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium. In the general population the incidence of pregnancy associated VTE is approximately 1 in 1500 deliveries The risk of VTE is five times higher in a pregnant than in a non-pregnant woman. Postpartum the VTE-risk is even higher. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose pregnancy-associated VTE clinically is generally poor, since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant of choice. In case of acute thrombosis during pregnancy, treatment is performed like in nonpregnant patients. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.
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PMID:Pregnancy-associated thrombosis. 1367 67

Venous thromboembolism occurs infrequently but is a leading cause of illness and death during pregnancy and the puerperium and remains a diagnostic and therapeutic challenge. In the general population the incidence of pregnancy associated VTE has been estimated to vary from 1 in 1000 to 1 in 2000 deliveries. The risk of VTE is five times higher in a pregnant woman than in a nonpregnant woman of similar age. Postpartum VTE is more common than antepartum VTE. Women with congenital abnormalities or persistent presence of antiphospholipid antibodies have an increased risk of VTE during pregnancy and the puerperium. In individuals with well defined hereditary thrombosis risk factors, such as the factor V:R506Q mutation, the factor II:G20210A variation, antithrombin-deficiency or protein C-deficiency, a relative risk of pregnancy associated VTE between 3.4 and 15.2 has been found. Women with previous VTE have an approximately 3.5 fold increased risk of recurrent VTE during pregnancy compared to non-pregnant periods. Our ability to diagnose deep-vein thrombosis clinically is generally poor and is further hampered during pregnancy since dyspnea, tachypnea, swelling and discomfort in the legs are common. Objective diagnosis is essential for treatment decisions. Exposure to radiation of less than 50,000 microGy (5 rad) has not been associated with a significant risk of fetal injury. Therefore, besides sonography, routine diagnostic procedures should be performed, if clinically necessary. Heparin does not cross the placenta and is therefore the anticoagulant treatment of choice during pregnancy. In case of acute new onset of thrombosis during pregnancy, treatment is performed like in non-pregnant patients with acute deep vein thrombosis or pulmonary embolism. There is ongoing debate, whether or not pregnant women with previous venous thrombosis should routinely receive prophylactic anticoagulation. In patients who have hereditary antithrombin deficiency, antiphospholipid antibodies, a combined abnormality or a history of a severe thrombotic event (pulmonary embolism, extended deep vein thrombosis) should be advised to use prophylactic heparin during pregnancy, starting during the first trimester. Post partum prophylaxis should be given in all women with an increased risk for VTE.
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PMID:Thrombosis during pregnancy: risk factors, diagnosis and treatment. 1367 66

By entrances to facilities, injury, invasions of the operation, and complication as cancer, etc., a crisis risk remarkably increases on pulmonary embolism thrombosis(PE). As risk factors of thrombosis except for above, abnormal protein C, abnormal protein S and abnormal antithrombin are often observed. Caucasians have frequently FV Leiden or abnormal FII as congenital thrombophilia, though those are not observed to Japanese. As an acquired risk factor for PE, there are cancer, high homocysteinemia, lipid abnormality and anti-phospholipid antibody syndrome. It is necessary to evaluate these risk factors for the prevention of PE.
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PMID:[Risk factors]. 1457 94

Paediatric patients with systemic lupus erythematosus (SLE) and antiphospholipid antibodies (aPL), specifically lupus anticoagulants (LAC) are at high risk of developing thromboembolic events (TE). Our objectives were to determine the prevalence of TE in paediatric SLE patients with LAC and to determine if anticoagulation was effective to decrease morbidity, and prevent recurrent TE. We reviewed data on 149 paediatric SLE patients treated over 10 years. In all, 24 patients (16%) were LAC positive, and 21 TE occurred in 13 of these LAC positive patients (54% incidence of TE in LAC positive patients). The events were cerebral venous thrombosis (9), arterial stroke (3), deep venous thrombosis (4), pulmonary embolism (2), other venous event (1) and other arterial events (2). The median duration between SLE diagnosis and first TE was 15.2 months (range 0-62), and the median age at first TE was 15.1 years (range 11.4-18.4). Long-term anticoagulation was prescribed, and eight patients (62%) were transferred to adult care on lifelong oral warfarin; four (31%) remain under our care on lifelong warfarin, and one patient died of causes unrelated to her TE. No patient has been identified with deficiencies of protein C, protein S or antithrombin III. One patient is heterozygous for Factor V Leiden, and one is heterozygous for both the Prothrombin 20210A mutation and the MTHFR (methylene tetrahydrofolate reductase) mutation. Four patients had recurrent TE (31%), and three were not anticoagulated at the time of their second event. One patient had two recurrences on therapeutic anticoagulation. Thromboembolic events are prevalent in the LAC positive paediatric SLE population, and consideration for lifelong anticoagulation must occur after an initial TE.
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PMID:Thromboembolism in paediatric lupus patients. 1459 22

Venous thromboembolism is a common and potentially fatal disease. If properly used, anticoagulation therapy is effective in preventing recurrence of venous thromboembolism and in improving survival. Symptomatic patients with an objective diagnosis of acute deep vein thrombosis (DVT) or pulmonary embolism (PE) should receive immediate systemic heparin anticoagulation at dosages sufficient to rapidly prolong the activated partial thromboplastin time into the laboratory-specific therapeutic range; this range corresponds to a plasma heparin concentration of 0.2 to 0.4 IU/ml (as measured by protamine sulfate titration), or 0.3 to 0.7 anti-Xa IU/ml. An oral vitamin K antagonist (e.g. warfarin) should be started within 24 hours after starting heparin; the starting dose should be the estimated patient-specific daily dose with no loading dose. Heparin and warfarin anticoagulation should be overlapped for at least 4 to 5 days and until the international normalized ratio (INR) is within the therapeutic range (2.0 to 3.0) on 2 measurements made at least 24 hours apart. The duration of warfarin anticoagulation should be individualized based on the respective risks of venous thromboembolism recurrence and anticoagulant-related bleeding. In general, warfarin should be continued for at least 3 months, and longer for patients with recurrent or idiopathic venous thromboembolism, malignant neoplasm, neurologic disease with extremity paresis, obesity, or laboratory evidence of a lupus anticoagulant/anticardiolipin antibody, homozygous carrier or combined heterozygous carrier for the factor V R506Q (Leiden) and prothrombin G20210A mutations, and possibly deficiency of either antithrombin, protein C, or protein S. Low molecular weight heparin (LMWH) is effective and well tolerated as acute therapy for patients with DVT or stable PE, and does not require laboratory monitoring or dose adjustment. Outpatient LMWH therapy is also well tolerated and cost effective for most patients with DVT, and possibly for selected patients with PE.
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PMID:Current management of acute symptomatic deep vein thrombosis. 1472 51

Venous thromboembolism (VTE) is one of the most frequent multifactorial diseases. It manifests clinically by deep vein thrombosis (DVT) and pulmonary embolism (PE) leading to death in about 6%. It is important to emphasize, that 50% of the patients do not present any symptoms. The prevalence is influenced by age and ethnics. Both, hereditary (Factor V Leiden, G20210A prothrombin gene mutation, deficiencies of protein C, S or antithrombin) and acquired risk factors (estrogen replacement, cancer, cardiovascular disease, surgery, trauma, immobility, use of central venous catheters, autoimmune disease such as anti-phospholipid syndrome) contribute to VTE. The risk increases dramatically by the addition of hyperhomocysteinemia or the combination of several risk factors. Since VTE is a dynamic process able to manifest clinically or to resolve completely, the identification of persons at increased risk is mainly important for early diagnosis and treatment. The diagnostic strategy including clinical scores and laboratory tests (D-dimer measurement) as initial steps to confirm the suspicion of VTE may exclude patients who do not need further, sometimes invasive imaging tests (venography, compression ultrasonography combined or not combined with colour Doppler imaging, magnetic resonance imaging). Laboratory tests for suspected inherited thrombophilia should be performed six months after clinical presentation.
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PMID:Epidemiology, etiology and diagnosis of venous thrombosis. 1509 18

A 53-year-old man with lung adenocarcinoma developed pulmonary embolism and bilateral popliteal venous thrombosis. Treated with intravenous unfractionated heparin and discharged home on warfarin, he returned a week later with extending thrombosis. Treatment with heparin followed by warfarin was reinitiated. Twenty-four hours following the re-administration of warfarin, the patient's INR increased to 14.5. The platelet count dropped by more than 50%, and he developed venous limb gangrene of the left leg and skin necrosis of the right leg. Heparin-induced thrombocytopenia was ruled out, and coagulation studies showed a severe depletion of protein C as well as increased thrombin generation. The patient was transfused with fresh frozen plasma, and vitamin K was given. Heparin was continued, and after 4 weeks, the patient improved markedly showing only minimal necrosis of the toes. Venous limb gangrene is a major complication associated with warfarin therapy. Its pathogenesis is explained by a transient hypercoagulable state produced by protein C depletion that leads to microvascular thrombi progressing to venous limb gangrene. The present case emphasizes the importance of careful anticoagulation with heparin followed by slow initiation of low-dose warfarin, in order to minimize thrombotic complications.
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PMID:Warfarin-induced limb gangrene in the setting of lung adenocarcinoma. 1516 86

The main objective of treatment of venous thromboembolism (VTE) is the prevention of the extension, embolization, and recurrence of thrombosis. The long-term aim is to prevent late recurrences and the post-thrombotic syndrome. Heparin and oral anticoagulants (OACs) have been the cornerstones of VTE treatment in the last 30 years. Low molecular weight heparins (LMWHs) have been introduced more recently in the treatment of the acute phase of VTE, and they have allowed the home treatment of deep vein thrombosis (DVT) in selected cases. The optimal duration of OAC therapy after VTE is still controversial. Several studies have been conducted, and several are ongoing with the aim to stratify patients into risk categories for recurrence. Patients at high risk are candidates for long-term oral anticoagulation as the benefits of extended oral anticoagulation would outweigh the risk of bleeding. Patients are currently stratified into risk categories on the basis of clinical characteristics of the VTE event: (1) first or recurrent event; (2) idiopathic or due to a transient risk factor such as surgery, trauma, hormonal therapy, or immobilization; (3) presence of active cancer; (4) location (proximal DVT and/or pulmonary embolism, PE, or distal DVT); and (5) presence of known hereditary or acquired thrombophilia. Patients with distal VTE or VTE due to a transient risk factor are at a low risk of recurrence and short-term anticoagulation is indicated (3 months). Patients with an idiopathic event or with known thrombophilic defects such as FV Leiden or the G20210A prothrombin mutation are candidates for a longer course of therapy (6 months). Patients with cancer, antiphospholipid antibodies syndrome, recurrent idiopathic event, antithrombin deficiency, protein C or protein S deficiency, homozygosity for FV Leiden, and double heterozygosity are candidates for extended long-term anticoagulation. More recently, studies have indicated that other factors such as D-dimer levels after the discontinuation of OAC therapy or the residual vein thrombosis could be additional predictive factors for recurrences. In patients with VTE and cancer, oral anticoagulation poses a higher risk of bleeding, and such patients are more prone to recurrences. Alternative treatment with LMWH could be safer and more effective in these patients.
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PMID:Oral anticoagulant therapy in venous thromboembolism. 1519 64

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